Matching and mismatching ventilation and perfusion in the lung

1996 ◽  
Vol 16 (3) ◽  
pp. 23-27 ◽  
Author(s):  
RS Misasi ◽  
JL Keyes

Arterial blood-gas composition is determined by ventilation, pulmonary blood flow, and by how ventilation is matched to blood flow in the lungs. In healthy adults there are regional differences in both ventilation and blood flow in the lungs and the distribution of blood flow tends to parallel that of ventilation. Ventilation and blood flow can become mismatched in a variety of disease processes that affect the lungs. Mismatching of ventilation and perfusion causes decreased PaO2, may change PaCO2, and increases AaDO2 difference. Many different types of interventions are frequently necessary to treat mismatching of ventilation and perfusion.

2014 ◽  
Vol 92 (5) ◽  
pp. 399-404 ◽  
Author(s):  
Romolo J. Gaspari ◽  
David Paydarfar

Atropine is used for a number of medical conditions, predominantly for its cardiovascular effects. Cholinergic nerves that innervate pulmonary smooth muscle, glands, and vasculature may be affected by anticholinergic medications. We hypothesized that atropine causes alterations in pulmonary gas exchange. We conducted a prospective interventional study with detailed physiologic recordings in anesthetized, spontaneously breathing rats (n = 8). Animals breathing a normoxic gas mixture titrated to a partial arterial pressure of oxygen of 110–120 were exposed to an escalating dose of intravenous atropine (0.001, 0.01, 0.1, 5.0, and 20.0 mg/kg body mass). Arterial blood gas measurements were recorded every 2 min (×5) at baseline, and following each of the 5 doses of atropine. In addition, the animals regional pulmonary blood flow was measured using neutron-activated microspheres. Oxygenation decreased immediately following intravenous administration of atropine, despite a small increase in the volume of inspired air with no change in respiratory rate. Arterial blood gas analysis showed an increase in pulmonary dysfunction, characterized by a widening of the alveolar–arteriole gradient (p < 0.003 all groups except for the lowest dose of atropine). The microsphere data demonstrates an abrupt and marked heterogeneity of pulmonary blood flow following atropine treatment. In conclusion, atropine was found to decrease pulmonary gas exchange in a dose-dependent fashion in this rat model.


1985 ◽  
Vol 59 (1) ◽  
pp. 254-261 ◽  
Author(s):  
W. M. Long ◽  
C. L. Sprung ◽  
H. el Fawal ◽  
L. D. Yerger ◽  
P. Eyre ◽  
...  

The effects of aerosolized 5% histamine (10 breaths) on bronchial artery blood flow (Qbr), airflow resistance (RL), and pulmonary and systemic hemodynamics were studied in mechanically ventilated sheep anesthetized with pentobarbital sodium. Histamine increased mean Qbr and RL to 252 +/- 45 and 337 +/- 53% of base line, respectively. This effect was significantly different from base line for 30 min after challenge. The histamine-induced increase in RL was blocked by pretreatment with the histamine H1 receptor antagonist, chlorpheniramine, whereas the histamine-induced elevation in Qbr was prevented by the H2 antagonist, metiamide. Both responses were blocked only when both antagonists were present. Changes in Qbr were not directly associated with alterations in systemic and pulmonary hemodynamics or arterial blood gas composition. In vitro histamine caused a dose-dependent contraction of ovine bronchial artery strips that was prevented by H1 antagonist. The H2 agonist, impromidine, caused relaxation of precontracted arterial strips and was more potent and efficacious than histamine, whereas H1 agonists failed to elicit a relaxant response. Thus these findings indicate that histamine aerosol induces a vasodilation in the bronchial vascular bed; histamine has a direct effect on Qbr that is independent of alterations in RL, systemic and pulmonary hemodynamics, or arterial blood gas composition; and, histamine-induced bronchoconstriction is mediated predominantly by H1-receptors, whereas increased Qbr is controlled predominantly by H2-receptors, probably located in resistance vessels. This local effect of histamine on Qbr may have important implications in the pathophysiology of bronchial asthma and pulmonary edema.


Children ◽  
2020 ◽  
Vol 7 (9) ◽  
pp. 137
Author(s):  
Amy Lesneski ◽  
Morgan Hardie ◽  
William Ferrier ◽  
Satyan Lakshminrusimha ◽  
Payam Vali

Background: The aim was to evaluate the relationship between the direction of the patent ductus arteriosus (PDA) shunt and the pre- and postductal gradient for arterial blood gas (ABG) parameters in a lamb model of meconium aspiration syndrome (MAS) with persistent pulmonary hypertension of the newborn (PPHN). Methods: PPHN was induced by intermittent umbilical cord occlusion and the aspiration of meconium through the tracheal tube. After delivery, 13 lambs were ventilated and simultaneous 129 pairs of pre- and postductal ABG were drawn (right carotid and umbilical artery, respectively) while recording the PDA and the carotid and pulmonary blood flow. Results: Meconium aspiration resulted in hypoxemia. The bidirectional ductal shunt had a lower postductal partial arterial oxygen tension ([PaO2] with lower PaO2/FiO2 ratio—97 ± 36 vs. 130 ± 65 mmHg) and left pulmonary flow (81 ± 52 vs. 133 ± 82 mL/kg/min). However, 56% of the samples with a bidirectional shunt had a pre- and postductal saturation gradient of < 3%. Conclusions: The presence of a bidirectional ductal shunt is associated with hypoxemia and low pulmonary blood flow. The absence of a pre- and postductal saturation difference is frequently observed with bidirectional right-to-left shunting through the PDA, and does not exclude a diagnosis of PPHN in this model.


1999 ◽  
Vol 36 (3) ◽  
pp. 431
Author(s):  
Tae Sook Park ◽  
Bong Il Kim ◽  
Jin Woong Park ◽  
Chan Hong Park ◽  
Woon Seok Roh ◽  
...  

1979 ◽  
Vol 290 (2) ◽  
pp. 163-184 ◽  
Author(s):  
B A Cross ◽  
B J Grant ◽  
A Guz ◽  
P W Jones ◽  
S J Semple ◽  
...  

2008 ◽  
Vol 32 (1) ◽  
pp. 61-64 ◽  
Author(s):  
Kent S. Kapitan

Students often have difficulty understanding the relationship of O2 consumption, CO2 production, cardiac output, and distribution of ventilation-perfusion ratios in the lung to the final arterial blood gas composition. To overcome this difficulty, I have developed an interactive computer simulation of pulmonary gas exchange that is web based and allows the student to vary multiple factors simultaneously and observe the final effect on the arterial blood gas composition (available at www.siumed.edu/medicine/pulm/vqmodeling.htm ). In this article, the underlying mathematics of the computer model is presented, as is the teaching strategy. The simulation is applied to a typical clinical case drawn from the intensive care unit to demonstrate the interdependence of the above factors as well as the less-appreciated importance of the Bohr and Haldane effects in clinical pulmonary medicine. The use of a computer to vary the many interacting factors involved in the arterial blood gas composition appeals to today's students and demonstrates the importance of basic physiology to the actual practice of medicine.


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